Phosphoinositide signalling and cardiac arrhythmias.
Arrhythmias arise from a complex interaction between structural changes in the myocardium and changes in cellular electrophysiology. Electrophysiological balance requires precise control of sarcolemmal ion channels and exchangers, many of which are regulated by phospholipid, phosphatidylinositol(4,5)bisphosphate. Phosphatidylinositol(4,5)bisphosphate is the immediate precursor of inositol(1,4,5)trisphosphate, a regulator of intracellular Ca2+ signalling and, therefore, a potential contributor to arrhythmogenesis by altering Ca2+ homeostasis. The aim of the present review is to outline current evidence that this signalling pathway can be a player in the initiation or maintenance of arrhythmias.
Woodcock
Elizabeth A
EA
Molecular Cardiology Laboratory, Baker IDI Heart and Diabetes Institute, PO Box 6492, St Kilda Road Central, Melbourne, 8008 Victoria, Australia. liz.woodcock@baker.edu.au
Kistler
Peter M
PM
Ju
Yue-Kun
YK
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D020013:Calcium Signaling / Q000502:physiology; D004195:Disease Models, Animal; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D051379:Mice; D010716:Phosphatidylinositols / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
D010716:Phosphatidylinositols; D015221:Potassium Channels